GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Wiley  (15)
  • Wang, Yan  (15)
  • 1
    Online Resource
    Online Resource
    Long non‐coding RNA LOC100133669 promotes cell proliferation in oesophageal squamous cell carcinoma
    Wiley ; 2020
    In:  Cell Proliferation Vol. 53, No. 4 ( 2020-04)
    Details
    In: Cell Proliferation, Wiley, Vol. 53, No. 4 ( 2020-04)
    Abstract: LOC100133669 is a lncRNA whose function during tumorigenesis remains unclear now. Thus, we aimed to explore its clinical significance and function in oesophageal squamous cell carcinoma (ESCC). Materials and Methods ISH was used to detect LOC100133669 expression in ESCC tissues. The full‐length LOC100133669 was identified by using RACE assay. Subcellular distribution of LOC100133669 was examined by nuclear/cytoplasmic RNA fractionation and qPCR. The role of LOC100133669 in ESCC cell growth was determined by colony formation, MTT and flow cytometry experiments in vitro, as well as xenograft tumour experiment in vivo. RNA pull‐down assay was performed to find LOC100133669‐interacted protein, which was further examined by RIP, IP, Western blot and rescue experiments. Results LOC100133669 was upregulated in ESCC tissues compared with adjacent non‐tumour tissues. High LOC100133669 expression was associated with poor prognosis of patients with ESCC. We defined LOC100133669 to be 831 nt in length and mainly localized in the cytoplasm of ESCC cells. Knockdown of LOC100133669 inhibited ESCC cell proliferation and cell cycle progression, while overexpression of LOC100133669 showed the opposite effects. Furthermore, LOC100133669 could bind to Tim50 and upregulated its protein level through inhibiting ubiquitination. Overexpression of Tim50 in part abolished the LOC100133669 depletion–caused inhibitory effect on ESCC cell proliferation. Conclusions LOC100133669 plays an oncogenic role in ESCC and may serve as a promising diagnostic marker and therapeutic target for ESCC patients.
    Type of Medium: Online Resource
    ISSN: 0960-7722 , 1365-2184
    URL: Issue
    URL: Article
    DOI: 10.1111/cpr.v53.4
    DOI: 10.1111/cpr.12750
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2019986-7
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Extracellular vesicles derived from oesophageal cancer containing P4HB promote muscle wasting via regulating PHGDH/Bcl‐2/caspase‐3 pathway
    Wiley ; 2021
    In:  Journal of Extracellular Vesicles Vol. 10, No. 5 ( 2021-03)
    Details
    In: Journal of Extracellular Vesicles, Wiley, Vol. 10, No. 5 ( 2021-03)
    Abstract: Cachexia, characterized by loss of skeletal muscle mass and function, is estimated to inflict the majority of patients with oesophageal squamous cell carcinoma (ESCC) and associated with their poor prognosis. However, its underlying mechanisms remain elusive. Here, we developed an ESCC‐induced cachexia mouse model using human xenograft ESCC cell lines and found that ESCC‐derived extracellular vesicles (EVs) containing prolyl 4‐hydroxylase subunit beta (P4HB) induced apoptosis of skeletal muscle cells. We further identified that P4HB promoted apoptotic response through activating ubiquitin‐dependent proteolytic pathway and regulated the stability of phosphoglycerate dehydrogenase (PHGDH) and subsequent antiapoptotic protein Bcl‐2. Additionally, we proved that the P4HB inhibitor, CCF642, not only rescued apoptosis of muscle cells in vitro, but also prevented body weight loss and muscle wasting in ESCC‐induced cachexia mouse model. Overall, these findings demonstrate a novel pathway for ESCC‐induced muscle wasting and advocate for the development of P4HB as a potential intervention target for cachexia in patients with ESCC.
    Type of Medium: Online Resource
    ISSN: 2001-3078 , 2001-3078
    URL: Issue
    URL: Article
    DOI: 10.1002/jev2.v10.5
    DOI: 10.1002/jev2.12060
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2683797-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Preventing BRCA 1/ ZBRK 1 repressor complex binding to the GOT2 promoter results in accelerated aspartate biosynthesis and promotion of cell proliferation
    Wiley ; 2019
    In:  Molecular Oncology Vol. 13, No. 4 ( 2019-04), p. 959-977
    Details
    In: Molecular Oncology, Wiley, Vol. 13, No. 4 ( 2019-04), p. 959-977
    Abstract: Breast cancer susceptibility gene 1 (BRCA1) has been implicated in modulating metabolism via transcriptional regulation. However, direct metabolic targets of BRCA 1 and the underlying regulatory mechanisms are still unknown. Here, we identified several metabolic genes, including the gene which encodes glutamate‐oxaloacetate transaminase 2 ( GOT 2), a key enzyme for aspartate biosynthesis, which are repressed by BRCA 1. We report that BRCA 1 forms a co‐repressor complex with ZBRK 1 that coordinately represses GOT 2 expression via a ZBRK 1 recognition element in the promoter of GOT2 . Impairment of this complex results in upregulation of GOT 2, which in turn increases aspartate and alpha ketoglutarate production, leading to rapid cell proliferation of breast cancer cells. Importantly, we found that GOT 2 can serve as an independent prognostic factor for overall survival and disease‐free survival of patients with breast cancer, especially triple‐negative breast cancer. Interestingly, we also demonstrated that GOT 2 overexpression sensitized breast cancer cells to methotrexate, suggesting a promising precision therapeutic strategy for breast cancer treatment. In summary, our findings reveal that BRCA 1 modulates aspartate biosynthesis through transcriptional repression of GOT 2, and provides a biological basis for treatment choices in breast cancer.
    Type of Medium: Online Resource
    ISSN: 1574-7891 , 1878-0261
    URL: Issue
    URL: Article
    DOI: 10.1002/mol2.2019.13.issue-4
    DOI: 10.1002/1878-0261.12466
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2322586-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    Focal adhesion kinase (FAK) inhibitor‐defactinib suppresses the malignant progression of human esophageal squamous cell carcinoma (ESCC) cells via effective blockade of PI3K/AKT axis and downstream molecular network
    Wiley ; 2021
    In:  Molecular Carcinogenesis Vol. 60, No. 2 ( 2021-02), p. 113-124
    Details
    In: Molecular Carcinogenesis, Wiley, Vol. 60, No. 2 ( 2021-02), p. 113-124
    Abstract: The clinical therapeutic efficacy toward esophageal squamous cell carcinoma (ESCC) is undesirable, due to the lack of targeted agents. Focal adhesion kinase (FAK), a nonreceptor tyrosine kinase involved in multiple fields of tumorigenesis, recently has been indicated as a promising therapeutic target in ESCC treatment. Here, we revealed that defactinib, a specific FAK inhibitor, effectively suppressed the malignancy of ESCC cells. Mechanistically, defactinib dose and time‐dependently induced the dissociation of phosphoinositide‐3‐kinase (PI3K) from FAK, resultantly led to blockade of protein kinase B (AKT) signaling, and the expression of several oncogenes, such as SOX2 , MYC , EGFR , MET , MDM2 , or TGFBR2 , identified by microarray and real‐time polymerase chain reaction assay. Specifically, this FAK inhibition‐mediated suppression of PI3K/AKT signaling and downstream ESCC specific biomarkers was maintained to 24 h in in vitro experiments to guarantee the treatment durability and efficacy. Importantly, defactinib suppressed tumor growth, metastatic ability, and increased overall survival of xenografted animals without producing significantly systematic toxicity. Our data suggest that FAK inhibition provides an excellent targeted therapy toward ESCC by effectively inhibiting PI3K/AKT pathway and downstream molecular network.
    Type of Medium: Online Resource
    ISSN: 0899-1987 , 1098-2744
    URL: Issue
    URL: Article
    DOI: 10.1002/mc.v60.2
    DOI: 10.1002/mc.23273
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2001984-1
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 5
    Online Resource
    Online Resource
    FAM135B sustains the reservoir of Tip60‐ATM assembly to promote DNA damage response
    Wiley ; 2022
    In:  Clinical and Translational Medicine Vol. 12, No. 8 ( 2022-08)
    Details
    In: Clinical and Translational Medicine, Wiley, Vol. 12, No. 8 ( 2022-08)
    Abstract: Recently, the mechanism by which cells adapt to intrinsic and extrinsic stresses has received considerable attention. Tat‐interactive protein 60‐kDa/ataxia–telangiectasia‐mutated (TIP60/ATM) axis‐mediated DNA damage response (DDR) is vital for maintaining genomic integrity. Methods Protein levels were detected by western blot, protein colocalisation was examined by immunofluorescence (IF) and protein interactions were measured by co‐immunoprecipitation, proximity ligation assay and GST pull‐down assays. Flow cytometry, comet assay and IF assays were used to explore the biological functions of sequence similarity 135 family member B (FAM135B) in DDR. Xenograft tumour, FAM135B transgenic mouse models and immunohistochemistry were utilised to confirm in vitro observations. Results We identified a novel DDR regulator FAM135B which could protect cancer cells from genotoxic stress in vitro and in vivo. The overexpression of FAM135B promoted the removal of γH2AX and 53BP1 foci, whereas the elimination of FAM135B attenuated these effects. Consistently, our findings revealed that FAM135B could promote homologous recombination and non‐homologous end‐joining repairs. Further study demonstrated that FAM135B physically bound to the chromodomain of TIP60 and improved its histone acetyltransferase activity. Moreover, FAM135B enhanced the interactions between TIP60 and ATM under resting conditions. Intriguingly, the protein levels of FAM135B dramatically decreased following DNA damage stress but gradually increased during the DNA repair period. Thus, we proposed a potential DDR mechanism where FAM135B sustains a reservoir of pre‐existing TIP60‐ATM assemblies under resting conditions. Once cancer cells suffer DNA damage, FAM135B is released from TIP60, and the functioning pre‐assembled TIP60‐ATM complex participates in DDR. Conclusions : We characterised FAM135B as a novel DDR regulator and further elucidated the role of the TIP60‐ATM axis in response to DNA damage, which suggests that targeting FAM135B in combination with radiation therapy or chemotherapy could be a potentially effective approach for cancer treatment.
    Type of Medium: Online Resource
    ISSN: 2001-1326 , 2001-1326
    URL: Issue
    URL: Article
    DOI: 10.1002/ctm2.v12.8
    DOI: 10.1002/ctm2.945
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2697013-2
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 6
    Online Resource
    Online Resource
    NiS Hollow Spheres for High-Performance Supercapacitors and Non-Enzymatic Glucose Sensors
    Wiley ; 2015
    In:  Chemistry - An Asian Journal Vol. 10, No. 3 ( 2015-03), p. 679-686
    Details
    In: Chemistry - An Asian Journal, Wiley, Vol. 10, No. 3 ( 2015-03), p. 679-686
    Type of Medium: Online Resource
    ISSN: 1861-4728
    URL: Article
    DOI: 10.1002/asia.201403198
    Language: English
    Publisher: Wiley
    Publication Date: 2015
    detail.hit.zdb_id: 2233006-9
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 7
    Online Resource
    Online Resource
    BAALC‐AS1/G3BP2/c‐Myc feedback loop promotes cell proliferation in esophageal squamous cell carcinoma
    Wiley ; 2021
    In:  Cancer Communications Vol. 41, No. 3 ( 2021-03), p. 240-257
    Details
    In: Cancer Communications, Wiley, Vol. 41, No. 3 ( 2021-03), p. 240-257
    Abstract: Long non‐coding RNAs (lncRNAs) have been found to be involved in the development of many cancers. In this study, we aimed to identify the molecular mechanisms of lncRNA BAALC antisense RNA 1 (BAALC‐AS1) in regulating the malignancy of esophageal squamous cell carcinoma (ESCC). Methods The expression of BAALC‐AS1 in cancer patients was analyzed using a tissue microarray. The protein and RNA levels of BAALC‐AS1 were determined by Western blotting analysis and quantitative reverse transcription‐PCR (RT‐qPCR), respectively. The cell proliferation was determined by cell viability assays, bromodeoxyuridine incorporation, and flow cytometry. The relationships among BAALC‐AS1, RasGAPSH3 domain‐binding protein 2 (G3BP2), and c‐Myc were determined using RNA immunoprecipitation, RNA pull‐down assays, and luciferase assays. Results The expression of BAALC‐AS1 was highly up‐regulated and associated with malignant phenotypes in ESCC tissues and cell lines. In vivo and in vitro assays showed that BAALC‐AS1 promoted ESCC cell proliferation, migration, and invasion. BAALC‐AS1 directly interacted with G3BP2, and thereby inhibited the degradation of c‐Myc RNA 3'‐UTR by G3BP2, thus leading to the accumulation of c‐Myc expression. Additionally, c‐Myc acted as a transcription factor that can induce the expression of BAALC‐AS1 by directly binding to its promoter region. Conclusions BAALC‐AS1/G3BP2/c‐Myc feedback loop plays a critical role in the development of ESCC, which might provide a novel therapeutic target and facilitate the development of new therapeutic strategies for the treatment of ESCC.
    Type of Medium: Online Resource
    ISSN: 2523-3548 , 2523-3548
    URL: Issue
    URL: Article
    DOI: 10.1002/cac2.v41.3
    DOI: 10.1002/cac2.12127
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2922913-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 8
    Online Resource
    Online Resource
    MAGE‐C3 promotes cancer metastasis by inducing epithelial‐mesenchymal transition and immunosuppression in esophageal squamous cell carcinoma
    Wiley ; 2021
    In:  Cancer Communications Vol. 41, No. 12 ( 2021-12), p. 1354-1372
    Details
    In: Cancer Communications, Wiley, Vol. 41, No. 12 ( 2021-12), p. 1354-1372
    Abstract: Evading immune surveillance is necessary for tumor metastasis. Thus, there is an urgent need to better understand the interaction between metastasis and mechanisms of tumor immune evasion. In this study, we aimed to clarify a novel mechanism that link tumor metastasis and immunosuppression in the development of esophageal squamous cell carcinoma (ESCC). Methods The expression of melanoma‐associated antigen C3 (MAGE‐C3) was detected using immunohistochemistry. Transwell assays were used to evaluate the migration and invasion ability of esophageal squamous cell carcinoma (ESCC) cells. Metastasis assays in mice were used to evaluate metastatic ability in vivo . Lymphocyte‐mediated cytotoxicity assays were performed to visualize the immune suppression function on tumor cells. RNA sequencing was performed to identify differentially expressed genes between MAGE‐C3 overexpressing ESCC cells and control cells. Gene ontology (GO) enrichment analyses was performed to identify the most altered pathways influenced by MAGE‐C3. The activation of the interferon‐γ (IFN‐γ) pathway was analyzed using Western blotting, GAS luciferase reporter assays, immunofluorescence, and flow cytometry. The role of MAGE‐C3 in the IFN‐γ pathway was determined by Western blotting and immunoprecipitation. Furthermore, immunohistochemistry and flow cytometry analysis monitored the changes of infiltrated T cell populations in murine lung metastases. Results MAGE‐C3 was overexpressed in ESCC tissues. High expression of MAGE‐C3 had a significant association with the risk of lymphatic metastasis and poor survival in patients with ESCC. Functional experiments revealed that MAGE‐C3 promoted tumor metastasis by activating the epithelial‐mesenchymal transition (EMT). MAGE‐C3 repressed antitumor immunity and regulated cytokine secretion of T cells, implying an immunosuppressive function. Mechanistically, MAGE‐C3 facilitated IFN‐γ signaling and upregulated programmed cell death ligand 1 (PD­L1) by binding with IFN‐γ receptor 1 (IFNGR1) and strengthening the interaction between IFNGR1 and signal transducer and activator of transcription 1 (STAT1). Interestingly, MAGE‐C3 displayed higher tumorigenesis in immune‐competent mice than in immune‐deficient nude mice, confirming the immunosuppressive role of MAGE‐C3. Furthermore, mice bearing MAGE‐C3‐overexpressing tumors showed worse survival and more lung metastases with decreased CD8 + infiltrated T cells and increased programmed cell death 1 (PD‐1) + CD8 + infiltrated T cells. Conclusion MAGE‐C3 enhances tumor metastasis through promoting EMT and protecting tumors from immune surveillance, and could be a potential prognostic marker and therapeutic target.
    Type of Medium: Online Resource
    ISSN: 2523-3548 , 2523-3548
    URL: Issue
    URL: Article
    DOI: 10.1002/cac2.v41.12
    DOI: 10.1002/cac2.12203
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2922913-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 9
    Online Resource
    Online Resource
    Feed‐forward activation of STAT3 signaling limits the efficacy of c‐Met inhibitors in esophageal squamous cell carcinoma (ESCC) treatment
    Wiley ; 2021
    In:  Molecular Carcinogenesis Vol. 60, No. 7 ( 2021-07), p. 481-496
    Details
    In: Molecular Carcinogenesis, Wiley, Vol. 60, No. 7 ( 2021-07), p. 481-496
    Abstract: c‐Hepatocyte growth factor receptor (Met) inhibitors have demonstrated clinical benefits in some types of solid tumors. However, the efficacy of c‐Met inhibitors in esophageal squamous cell carcinoma (ESCC) remains unclear. In this study, we discovered that c‐Met inhibitors induced “Signal Transducer and Activator of Transcription (STAT3)‐addiction” in ESCC cells, and the feedback activation of STAT3 in ESCC cells limits the tumor response to c‐Met inhibition. Mechanistically, c‐Met inhibition increased the autocrine of several cytokines, including CCL2, interleukin 8, or leukemia inhibitory factor, and facilitated the interactions between the receptors of these cytokines and Janus Kinase1/2 (JAK1/2) to resultantly activate JAKs/STAT3 signaling. Pharmacological inhibition of c‐Met together with cytokines/JAKs/STAT3 axis enhanced cancer cells regression in vitro. Importantly, combined c‐Met and STAT3 inhibitors synergistically suppressed tumor growth and promoted the apoptosis of tumor cells without producing systematic toxicity. These findings suggest that inhibition of the STAT3 feedback loop may augment the response to c‐Met inhibitors via the STAT3‐mediated oncogene addiction in ESCC cells.
    Type of Medium: Online Resource
    ISSN: 0899-1987 , 1098-2744
    URL: Issue
    URL: Article
    DOI: 10.1002/mc.v60.7
    DOI: 10.1002/mc.23306
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2001984-1
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 10
    Online Resource
    Online Resource
    NOX5 mediates the crosstalk between tumor cells and cancer‐associated fibroblasts via regulating cytokine network
    Wiley ; 2021
    In:  Clinical and Translational Medicine Vol. 11, No. 8 ( 2021-08)
    Details
    In: Clinical and Translational Medicine, Wiley, Vol. 11, No. 8 ( 2021-08)
    Abstract: Activation of cancer‐associated fibroblasts (CAFs) is a crucial feature for tumor malignancy. The reciprocal interplay between tumor cells and CAFs not only facilitates tumor progression and metastasis but also sustains the tumor‐promoting function of CAFs. Nevertheless, how tumor cells readily adapt to these functional CAFs is still unclear. NADPH oxidase 5 (NOX5) is a strong reactive oxygen species producer overexpressed in esophageal squamous cell carcinoma (ESCC) cells. In this study, we showed that NOX5‐positive ESCC cells induced normal fibroblasts (NFs) or adipose‐derived mesenchymal stem cells (MSCs) to express the marker of CAFs‐α smooth muscle actin. Moreover, these tumor cells reprogrammed the cytokine profile of the activated CAFs, which further stimulated NFs or MSCs to CAFs and induced lymphangiogenesis to facilitate ESCC malignancy. NOX5 activated intratumoral Src/nuclear factor‐κB signaling to stimulate secretion of tumor necrosis factor‐α (TNF‐α), interleukin‐1β (IL‐1β), and lactate from tumor cells. Subsequently, TNF‐α, IL‐1β, and lactate activated CAFs, and facilitated the secretion of IL‐6, IL‐7, IL‐8, CCL5, and transforming growth factor‐β1 from CAFs. These CAFs‐derived cytokines reciprocally induced the progression of NOX5‐positive ESCC cells. Our findings together indicate that NOX5 serves as the driving oncoprotein to provide a niche that is beneficial for tumor malignant progression.
    Type of Medium: Online Resource
    ISSN: 2001-1326 , 2001-1326
    URL: Issue
    URL: Article
    DOI: 10.1002/ctm2.v11.8
    DOI: 10.1002/ctm2.472
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2697013-2
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...